Spectrum of medial medullary infarction: clinical and magnetic resonance imaging findings.

Among 4200 consecutive patients admitted to three hospitals with acute ischemic stroke, we found only 11 patients in whom magnetic resonance imaging (MRI) had proved that they had medial medullary infarction (MMI). In our centers, patients with MMI were less than 1% of those with vertebrobasilar stroke. The infarcts documented by MRI were unilateral in 10 patients and bilateral in one. On clinico-topographical analysis there were four clinical patterns: (1) Classical Dejerine's syndrome was the most frequent, consisting of contralateral hemiparesis, lemniscal sensory loss and ipsilateral lingual palsy in 7 of the eleven patients. (2) Pure hemiparesis was present in 2 patients; (3) Sensorimotor stroke was present in 1 patient with contralateral hemiparesis, hypesthesia and mild decrease in pain sensation without lingual palsy; (4) Bilateral MMI syndrome in 1 patient, accompanied by tetraparesis, bilateral loss of deep sensation, dysphagia, dysphonia and anarthria. Presumed causes of MMI were intrinsic branch penetrator artery disease with concomitant vertebral artery stenosis in 6 of the 11 patients, vertebral artery occlusion in 2, dolichoectatic vertebrobasilar arteries in 2, a source of cardiac embolism in 1. Prognosis at 3 months was favorable in 8 patients, but the patient with bilateral MMI syndrome had persisting motor deficit causing limitation of daily activities, and 2 died from systemic causes. The classical triad of acute MMI facilitates the diagnosis, although the recognition of this syndrome in patients with incomplete manifestations can be difficult and occurs more frequently than commonly thought. Moreover, vertebral artery atherosclerosis and branch atheromatous disease of the penetrating arteries are the main causes of medullary infarction.

Microembolus detection in patients with Takayasu's arteritis.

BACKGROUND AND PURPOSE: Takayasu's arteritis (TA) is a chronic inflammatory disease of unknown etiology that can affect the aorta and its branches. The cerebral ischemia in TA can be caused by a variety of mechanisms, and the focus of this study is to detect the possible contribution of microembolus in the pathogenesis of stroke. METHODS: Eighteen patients with TA according to the criteria for the classification of TA of the American College of Rheumatology and 100 age-matched healthy controls were studied. Both middle cerebral arteries were monitored by transcranial Doppler (TCD) ultrasound for at least 30 minutes. All patients with TA were followed up for a mean duration of 2.1 months, and recurrent strokes were registered. RESULTS: Microembolic signals (MES) were present in 22% of the patients overall, and the intensity of the MES varied between 9 and 30 dB. Moreover, MES were found in 30% of the patients with higher erythrocyte sedimentation rate. Two (67%) of 3 patients who did not receive any treatment had MES, but only 2 (13%) of 15 patients who received immunosuppressive and anticoagulant therapy before the TCD ultrasonography monitoring had MES. During the follow-up period after MES recording, we did not observe any recurrent stroke. CONCLUSIONS: TCD ultrasonography monitoring can be used as an additional noninvasive procedure to detect microembolus in patients with TA during the acute and chronic phase of the disease. The monitoring of MES may also help in choosing better treatment for the long-term prophylaxis of the disease from acute ischemic stroke, but further large studies are required to justify the efficacy of immunosuppressive treatment in these patients.

Detection of microembolic signals in patients with neuropsychiatric lupus erythematosus.

The pathogenesis of central nervous system involvement in systemic lupus erythematosus (SLE) is not completely understood. In this study, we investigated the association of microembolic signals (MES) with a variety of neuropsychiatric SLE manifestations and compared our results with those from SLE patients without neuropsychiatric lupus and normal controls. Fifty-three patients with SLE (45 females and 8 males), all fulfilling the revised classification criteria for SLE, and 50 control subjects (44 females and 6 males) were enrolled in this study. All SLE patients were assessed by neuropsychological examination, including various neuropsychiatric tests. Twenty-five patients with SLE were found to have at least one of the neuropsychiatric syndromes defined by The American College of Rheumatology. The mean MES count in patients with neuropsychiatric lupus was significantly higher than those without (5.4 +/- 1.1 vs. 0.3 +/- 0.8/h; p < 0.005). We found a positive correlation between higher mean MES counts and the presence of neuropsychiatric syndromes in SLE. The mean MES count in the whole group of SLE patients was also significantly higher than that in healthy controls. The mean MES count of SLE patients with antiphospholipid (aPL) antibody positivity was significantly higher than those without aPL antibodies (3.6 +/- 1.6 vs. 0.8 +/- 0.1/h; p < 0.005). In conclusion, the association of MES with neuropsychiatric lupus may support the possible contribution of MES to the complex pathophysiology of this syndrome. More importantly, detection of MES on transcranial Doppler monitoring might suggest a high risk of involvement of the central nervous system in SLE, and could be used as a diagnostic tool.